This study will continue animal research designed to model the problem of sudden death after repair of congenital heart defects such as tetralogy of Fallot (TOF). Patients who have died suddenly had the combination of ventricular arrhythmias (VA) and elevated right ventricular (RV) systolic and end-diastolic pressures. The specific aims of this study are to determine in an animal model: (1) the anatomic and physiologic conditions necessary for the development of VA; 2) the cellular electrophysiologic mechanism for the VA. Our previous animal research has suggested a mechanism of triggered activity; 3) the mechanism of sudden death. We have completed studies on three groups of "unrepaired" beagle puppies, control, chronic RV hypertrophy and chronic right ventriculotomy, and demonstrated, as postulated, normal cellular electrophysiology and no inducible VA. However, in response to rapid V pacing (simulating ventricular tachycardia, (VT) the animals with the chronic PA band developed reduced coronary blood flow and elevated serum norepinephrine thus providing a possible mechanism for ventricular fibrillation following spontaneous VT. In the period covered by this renewal application, we will create a model of " preoperative" cyanotic TOF and later perform "correction". All four groups of animals will have at the age of 6 weeks PA banding and PA to LA anastomosis: at 6 mos: Gp 1-right ventriculotomy and combinations of PS with or without PI; Gp 2-no ventriculotomy; Gp 3-central right bundle branch block; Gp 4-no myocardial protection. For 6 mos after each "correction" every 2 wks, the animals will have electrophysiology study and 24-hr ECG. At the end of this time, the hemodynamic response of the unsedated animal simulated tachyarrhythmias will be examined as well as blood flows with radioactive microspheres; then microelectrode studies will be done on the excised heart. The significance is: 1) if certain residual hemodynamic abnormalities are found to be associated with VA, they could be avoided; 2) if a specific mechanism for VA due to hypertrophy and dilation is found, this might extend to lesions such as aortic stenosis/aortic insufficiency or systemic hypertension. The difference in mechanism could account for the difference in drug response between children and adults with VA; 3) if the VA mechanism involves triggered activity, this would be the first chronic animal model of this mechanism; 4) if the explanation for sudden death from VA can be found, this will benefit both children and adults since it might be possible to predict which patients will die suddenly.